Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Human Polyclonal Oncostatin M Primary Antibody for CyTOF, FACS - ABIN4899954
Ohsaka, Hirota-Komatsu, Shibata, Ezaki, Shinohara, Yoshida: Specific association of increased vascular endothelial growth factor expression and its receptors with macrophage differentiation of HL-60 leukemia cells. in Biochemical and biophysical research communications 2008
Show all 2 Pubmed References
Human Polyclonal Oncostatin M Primary Antibody for IHC, IHC (p) - ABIN4341425
Guo, Chen, Shi, Wang, Chen, Diao, Hu, Yu, Qian, Guo: Stat3-coordinated Lin-28-let-7-HMGA2 and miR-200-ZEB1 circuits initiate and maintain oncostatin M-driven epithelial-mesenchymal transition. in Oncogene 2013
Human Polyclonal Oncostatin M Primary Antibody for ELISA (Detection), FACS - ABIN4899952
Hurst, McLoughlin, Monslow, Owens, Morgan, Fuller, Topley, Jones: Secretion of oncostatin M by infiltrating neutrophils: regulation of IL-6 and chemokine expression in human mesothelial cells. in Journal of immunology (Baltimore, Md. : 1950) 2002
Human Monoclonal Oncostatin M Primary Antibody for IHC, IHC (p) - ABIN4341424
Kang, Kim, Jang, Park, Lee, Kim: 22q11-q13 as a hot spot for prediction of disease-free survival in bile duct cancer: integrative analysis of copy number variations. in Cancer genetics 2014
Oncostatin M induces RIG-I (show DDX58 Antibodies) and MDA5 (show IFIH1 Antibodies) expression and enhances the double-stranded RNA response in fibroblasts.
The IL-6 (show IL6 Antibodies)-type cytokine oncostatin M (OSM) indeed induces cellular properties associated with tumorigenesis and disease progression in non-transformed human prostate epithelial cells, including morphological changes, epithelial-to-mesenchymal transition (EMT (show ITK Antibodies)), enhanced migration and pro-invasive growth patterns.
downregulation of miR (show MLXIP Antibodies)-20a-5p is caused by promoter hypermethylation. MiR (show MLXIP Antibodies)-20a-5p could also suppress the production of IL-17 (show IL17A Antibodies) by targeting OSM and CCL1 (show CCL1 Antibodies) production in CD4 (show CD4 Antibodies)(+) T cells in patients with active VKH.
our findings suggested that OSM suppresses SLUG expression and tumor metastasis of lung adenocarcinoma cells through inducing the inhibitory effect of the STAT1 (show STAT1 Antibodies)-dependent pathway and suppressing the activating effect of STAT3 (show STAT3 Antibodies)-dependent signaling
Genistein (a specific Tyr (show TYR Antibodies) phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein (show DDIT3 Antibodies)) with C/EBP-beta (show CEBPB Antibodies), thus negatively regulating it. Knockdown of C/EBP-beta (show CEBPB Antibodies) also leads to inhibition of PMA-mediated OSM induction.
Data provide evidence that OSM regulates an epithelial-mesenchymal transition and cancer stem cell plasticity program that promotes tumorigenic properties in pancreatic cells.
OSM-induced plasticity was Signal Transducer and Activator of Transcription 3 (STAT3 (show STAT3 Antibodies))-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD (show SMAD1 Antibodies) signaling. Removal of OSM or inhibition of STAT3 (show STAT3 Antibodies) or SMAD3 (show SMAD3 Antibodies) resulted in a marked reversion to a non-invasive, epithelial phenotype.
Neutrophils are a major source of OSM-producing cells in patients with chronic rhinosinusitis and severe asthma.
OSM and OSMR are highly expres (show TNF Antibodies)sed in inflammatory bowel disease intestinal mucosa compared to control mucosa. OSM promotes inflammatory behavior in human intestinal stroma.
Study showed that in atrial fibrillation (AF) with thrombus, the atrial tissue infiltration of M1 macrophages increased significantly; the OSM expression was also found to increase simultaneously; downstream tissue factor (show F3 Antibodies) (TF) increased and tissue factor (show F3 Antibodies) pathway inhibitors (TFPI (show TFPI Antibodies))decreased, leading to an imbalance between TF and TFPI (show TFPI Antibodies) eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI (show TFPI Antibodies)
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A Antibodies) and IL-21 (show IL21 Antibodies); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3 (show SOCS3 Antibodies)), STAT3 (show STAT3 Antibodies), and STAT5 (show STAT5A Antibodies); observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3 (show SOCS3 Antibodies), STAT3 (show STAT3 Antibodies), and STAT5 (show STAT5A Antibodies)
In an animal model of anti-TNF (show TNF Antibodies)-resistant intestinal inflammation, genetic deletion or pharmacological blockade of OSM significantly attenuates colitis.
these results support the proinflammatory role of OSM when it is overexpressed in the skin. However, OSM expression was not required in the murine model of psoriasis induced by topical application of imiquimod, as demonstrated by the inflammatory phenotype of OSM-deficient mice or wild-type mice treated with anti-OSM antibodies.
OSM (mOSM) signals mainly via an OSM receptor (OSMR)-gp130 heterodimer and binds with only very low affinity to mLIFR.
Loss of Oncostatin M Signaling in Adipocytes Induces Insulin (show INS Antibodies) Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf (show SNRPE Antibodies)/Mek (show MDK Antibodies)/Erk (show EPHB2 Antibodies) signaling pathway through the OSM receptor Obeta
Oncostatin M and interleukin-31 (show IL31 Antibodies): Cytokines, receptors, signal transduction and physiology.
OSM plays multiple critical roles in the maintenance and development of the hematopoietic microenvironment in the bone marrow at a steady state as well as after injury.
OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF (show VEGFA Antibodies) and bFGF (show FGF2 Antibodies) in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI.
The mechanism of Oncostatin M on cardiac ischemia/reperfusion injury is partly mediated by the Notch3 (show NOTCH3 Antibodies)/Akt (show AKT1 Antibodies) pathway.
Protein kinase R plays a pivotal role in oncostatin M and interleukin-1 signalling in bovine articular cartilage chondrocytes.
Oncostatin M is a member of a cytokine family that includes leukemia-inhibitory factor, granulocyte colony-stimulating factor, and interleukin 6. This gene encodes a growth regulator which inhibits the proliferation of a number of tumor cell lines. It regulates cytokine production, including IL-6, G-CSF and GM-CSF from endothelial cells.